ABSTRACT
Chronic exposure in a low-O2 environment (i.e., chronic hypoxia, CH) initiates a multitude of physiological adjustments that tend to mitigate the adverse effects of hypoxia. These homeostatic mechanisms involve multiple sensory and hormonal factors acting locally and systemically to increase the capacity and efficiency of O2 delivery and utilization. Among the most important of the changes is increased ventilation, evident as elevated tidal volume and/or frequency of breathing. During acute hypoxia, breathing increases to a new steady-state level. However, if hypoxia continues for hours or days, a further progressive increase in ventilation occurs, until a second steady-state level is established (1). Such ventilatory acclimatization to hypoxia (VAH), develops in rats and humans over a 4-5-day period, and the elevated breathing persists for at least 14 days (2). Recent data indicate that VAH involves adjustments both in the central processing of sensory input (3,4) and the generation of chemoreceptor activity in the carotid body. Indeed, quantitative studies of carotid sinus nerve (CSN) activity have demonstrated increased carotid body hypoxic chemosensitivity following prolonged exposure to hypoxia (5-8). Importantly, the time course of these changes in carotid body function parallels the development of VAH (9).
